Effect of prostaglandin E 2 on central and peripheral catecholamine neurons

Abstract

Effects of prostaglandin E 2 (PGE 2) on catecholamine (CA) release from CA neurons have been studied in two models; influence on field stimulation-induced overflow of tritium from isolated tissues pre-incubated with 3H-CA; influence on dopamine (DA) disappearance in the neostriatum induced by tyrosine hydroxylase inhibition utilizing histochemical fluorescence analysis of catecholamines. In vitro PGE 2 (3 × 10 −6 M) caused a small but probably significant reduction of the field stimulation-induced tritium overflow from central noradrenaline (NA) and central DA nerve terminals and a significant reduction of the stimulation-induced overflow from peripheral NA nerve terminals. In the in vivo experiments PGE 2 in μg amounts was dissolved in Krebs-Ringer bicarbonate buffer and infused into the left neostriatum, whereas buffer alone was infused into the right neostriatum. Infusion of 9–18 μg of PGE 2 reduced the disappearance of DA fluorescence after treatment with the tyrosine hydroxylase inhibitor α-methyl-tyrosine methylester ( H 44 68 ) under resting conditions, but could not counteract the increase in H 44 68 - induced DA disappearance caused by electrical stimulation of the nigro-neostriatal DA pathway. The findings suggest that PGE 2 can modify but not stop the release of DA and NA from central CA nerve terminals and indicate that prostaglandins might act as modulators of central CA neurotransmission.